Abstract
The sulfate reducing bacterium Desulfovibrio desulfuricans inhabits both the human gut and external environments. It can reduce nitrate and nitrite as alternative electron acceptors to sulfate to support growth. Like other sulphate reducing bacteria, it can also protect itself against nitrosative stress caused by NO generated when nitrite accumulates. By combining in vitro experiments with bioinformatic and RNA-seq data, metabolic responses to nitrate or NO and how nitrate and nitrite reduction are coordinated with the response to nitrosative stress were revealed. Although nitrate and nitrite reduction are tightly regulated in response to substrate availability, the global responses to nitrate or NO were largely regulated independently. Multiple NADH dehydrogenases, transcription factors of unknown function and genes for iron uptake were differentially expressed in response to electron acceptor availability or nitrosative stress. Amongst many fascinating problems for future research, the data revealed a YtfE orthologue, Ddes_1165, that is implicated in the repair of nitrosative damage. The combined data suggest that three transcription factors coordinate this regulation in which NrfS-NrfR coordinates nitrate and nitrite reduction to minimize toxicity due to nitrite accumulation, HcpR1 serves a global role in regulating the response to nitrate, and HcpR2 regulates the response to nitrosative stress.
Highlights
Many strains of sulfate reducing bacteria such as Desulfovibrio vulgaris that have been isolated from natural environments outside warm blooded animals lack genes for nitrate reduction, but with few exceptions, they are able to reduce nitrite to ammonia[1,2,3,4,5,6,7,8]
We recently showed that hybrid cluster protein (Hcp) in enteric bacteria is a high affinity nitric oxide reductase that protects cytoplasmic proteins from nitrosative damage by NO generated as a side product of nitrite reduction to ammonia[22]
Two of the 5 transcription factors of the Crp-FNR family encoded in the D. desulfuricans 27774 genome, HcpR1 and HcpR2, are both predicted to regulate the response to nitrosative stress
Summary
Many strains of sulfate reducing bacteria such as Desulfovibrio vulgaris that have been isolated from natural environments outside warm blooded animals lack genes for nitrate reduction, but with few exceptions, they are able to reduce nitrite to ammonia[1,2,3,4,5,6,7,8]. Homologues of genes that protect bacteria from nitrosative stress can be identified in the genomes of sulfate reducing bacteria[15,16,18,19,20,21] They include transcription factors such as HcpR and genes that they regulate such as hcp encoding the hybrid cluster protein, Hcp. We recently showed that Hcp in enteric bacteria is a high affinity nitric oxide reductase that protects cytoplasmic proteins from nitrosative damage by NO generated as a side product of nitrite reduction to ammonia[22]. A fascinating result from the previous study was that NO induced expression of the hcp and hcpR1 genes, HcpR2 was shown to be the transcription factor that regulates Hcp synthesis, but hcpR2 transcription is not induced by NO
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